2016 Fiscal Year Final Research Report
Mg2+ regulation by SLC41 transporters and pathological mechanism for its abnormality
| Project/Area Number |
26460351
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KITA Satomi 福岡大学, 医学部, 准教授 (10461500)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | イオン輸送体 / マグネシウム / 病態モデル |
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| Outline of Final Research Achievements |
Cellular Mg2+ plays an important role in various cellular functions, such as energy metabolism, channel activity, and enzyme activity. Therefore, various diseases are caused by abnormal Mg2+ regulation. Recently, several Mg2+ transporters are cloned, but their functional roles are still well unknown. We first observed that the expression levels of SLC41 transporters in aorta were dependent on the Mg2+ intake (low, normal, or high). In addition, we found that phenylephrine-induced contraction was reduced in isolated aorta from low-magnesium-fed mice. Furthermore, we next generated SLC41A1/A2-knockout mice. Interestingly, phenylephrine-induced contraction was reduced in isolated aorta from SLC41A2-knockout mice fed with normal-magnesium diet. These results suggest that SLC41A1/A2 play an important role in vascular function. Further work will be required to define the pathological role of SLC41A1/A2 in cardiovascular diseases.
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| Free Research Field |
膜輸送体
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